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Regulation of parasite‐specific antibody responses in resistant (C57BL/6) and susceptible (C3H/HE) mice infected with Trypanosoma (trypanozoon) brucei brucei
Author(s) -
BLACK S. J.,
SENDASHONGA C. N.,
WEBSTER P.,
KOCH G. L. E.,
SHAPIRO S. Z.
Publication year - 1986
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/j.1365-3024.1986.tb00859.x
Subject(s) - biology , trypanosoma brucei , parasite hosting , virology , trypanosoma , kinetoplastida , parasitology , antibody , immunology , microbiology and biotechnology , protozoal disease , zoology , genetics , gene , world wide web , computer science , malaria
Summary After infection with 10 3 T. brucei GUTat 31, C57BL/6 mice produced antibody responses and controlled the first parasitaemic wave whereas C3H/Hemice did not. The inability of C3H/He mice to control parasitaemia resulted from an impaired ability of parasite‐induced antibody‐containing cells to secrete immunoglobulin. Antibody‐containing cells in infected C3H/He mice regained the ability to secrete antibody within 24 h after trypanosome elimination by treatment with Berenil, suggesting that the block in antibody secretion was maintained by living parasites or short‐lived components of degenerating parasites. Infected C3H/He mice also had an impaired ability to produce a rabbit erythrocyte‐specific antibody response on challenge with rabbit erythrocytes and this response recovered when parasites were eliminated from the blood 24 h before analysis. It was not possible to inhibit secretion of antibody by rabbit erythrocyte‐induced plasma cells either by incubating them with serum from infected C3H/He mice or by injecting large numbers of living trypanosomes into C3H/He mice already responding to rabbit erythrocytes. The process leading to failure of parasite and rabbit erythrocyte‐induced antibody‐containing cells to become high rate antibody‐secreting cells was not identified but did not appear to correlate with any obvious change in the intra‐cellular morphology of the antibody‐containing cells.